Attention deficit hyperactivity disorder (ADHD) and obesity: Two facets of the same disease?

Summary

We hypothesize that when two pathological conditions or personality traits share the same critical period for gene–environment interaction, we should expect further similarities, particularly from clinical and pathophysiological perspectives. They should therefore be considered as two facets of the same disease. To test this hypothesis we compiled data included in the Primal Health Research Database. This database (www.primalhealthresearch.com) is specialised in studies exploring correlations between what happens during the ‘primal period’ (fetal life, perinatal period and year following birth) and what happens later on in life in terms of health and personality traits. After mentioning the links between autism and anorexia nervosa, we explore more in depth the links between attention deficit hyperactivity disorder (ADHD) and obesity. We suggest from such examples that the nature of an environmental factor is often less important than the timing of the interaction. We conclude that the concept of gene expression, combined with Primal Health Research, might lead to reconsider conventional nosological classifications. Some previously well-defined pathological entities should be included into the framework of multifaceted diseases. On the other hand some existing pathological entities should be dismantled.

Introduction

Until now, nosology was based on descriptions of symptoms (e.g. scarlet fever), on altered functions (e.g. hyperthyroidism), on altered organs (e.g. myocardial infarction), or on the name of a physician who described the pathological entity (e.g. Addison’s disease). Today, the Primal Health Research Database (www.primalhealthresearch.com) suggests new ways to classify diseases [1]. Classification is now possible according to critical periods for gene–environment interaction. When two conditions seem to be similar with regard to timing for such interactions, we can go beyond the concept of co-morbidity to explore other possible similarities, particularly from clinical and pathophysiological perspectives. This is how, after studying in parallel anorexia nervosa and autism, two entities with similar critical periods for gene–environment interaction, we suggested that anorexia nervosa might be considered a female variant of the autistic spectrum [2]. A plausible interpretation of why anorexia nervosa is undoubtedly seen more in females is that prenatal exposure to male hormones might protect against the expression of this disease. A study of twins suggests such an interpretation. Girls who have a twin brother are at low risk for anorexia nervosa, compared with girls who have a twin sister, and with controls [3]. This interpretation is reinforced by the negative results of genetic linkage analyses that detected no change on the X chromosome [4]. Not only can Primal Health Research establish links between pathological entities, but it can also dismantle existing entities. For example, the Primal Health Research perspective significantly differentiates subjects with anorexia nervosa from those with bulimia nervosa and suggests that the broad concept of ‘eating disorder’ should be reconsidered.

We shall use the same method to explore possible links between ADHD and obesity.